PMID- 28327409
OWN - NLM
STAT- MEDLINE
DCOM- 20170710
LR  - 20220317
IS  - 1090-2422 (Electronic)
IS  - 0014-4827 (Linking)
VI  - 354
IP  - 2
DP  - 2017 May 15
TI  - MiR-23a-5p modulates mycobacterial survival and autophagy during mycobacterium 
      tuberculosis infection through TLR2/MyD88/NF-kappaB pathway by targeting TLR2.
PG  - 71-77
LID - S0014-4827(17)30151-9 [pii]
LID - 10.1016/j.yexcr.2017.03.039 [doi]
AB  - Autophagy plays a pivotal role in activating the antimicrobial host defense 
      against Mycobacterium tuberculosis (M.tb.). The emerging roles of microRNAs 
      (miRNAs) in regulating immune responses have attracted increasing attention in 
      recent years. Appreciating the potential of host-directed therapies designed to 
      control autophagy during mycobacterial infection, we focused on the influence of 
      miR-23a-5p on the activation of macrophage autophagy during M.tb. infection in 
      bone marrow-derived macrophages (BMDMs) and murine RAW264.7 cells. Here, we 
      demonstrated that M.tb.-infection of macrophages lead to markedly enhanced 
      expression of miR-23a-5p in a time- and dose-dependent manner. Furthermore, 
      forced expression of miR-23a-5p accelerated the survival rate of intracellular 
      mycobacteria, while transfection with miR-23a-5p inhibitors attenuated 
      mycobacterial survival. More importantly, overexpression of miR-23a-5p 
      dramatically prevented M.tb.-induced activation of autophagy in macrophages, 
      whereas inhibitors of miR-23a-5p remarkably accelerated M.tb.-induced autophagy. 
      Mechanistically, miR-23a-5p is able to modulate TLR2/MyD88/NF-kappaB signaling 
      activity by targeting TLR2 in RAW264.7 cells in response to M.tb.-infection. 
      Collectively, these findings demonstrated that miR-23a-5p modulated the innate 
      host defense by promoting mycobacteria survival and inhibiting the activation of 
      autophagy against M.tb. through TLR2/MyD88/NF-kappaB pathway by targeting TLR2, which 
      may provide a promising therapeutic target for tuberculosis.
CI  - Copyright (c) 2017 Elsevier Inc. All rights reserved.
FAU - Gu, Xing
AU  - Gu X
AD  - Respiratory and Critical Care Medicine, Tangdu Hospital, The Fourth Military 
      Medical University, No. 1 Xinsi Road, Xi'an 710038, Shaanxi, PR China.
FAU - Gao, Yan
AU  - Gao Y
AD  - Department of Respiratory Medicine, People's Hospital of BaoJi City, Baoji 
      721000, Shaanxi, PR China.
FAU - Mu, De-Guang
AU  - Mu DG
AD  - Respiratory and Critical Care Medicine, Tangdu Hospital, The Fourth Military 
      Medical University, No. 1 Xinsi Road, Xi'an 710038, Shaanxi, PR China. Electronic 
      address: deguang@fmmu.edu.cn.
FAU - Fu, En-Qing
AU  - Fu EQ
AD  - Respiratory and Critical Care Medicine, Tangdu Hospital, The Fourth Military 
      Medical University, No. 1 Xinsi Road, Xi'an 710038, Shaanxi, PR China. Electronic 
      address: enqingfu66@163.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20170319
PL  - United States
TA  - Exp Cell Res
JT  - Experimental cell research
JID - 0373226
RN  - 0 (3' Untranslated Regions)
RN  - 0 (MicroRNAs)
RN  - 0 (Mirn23b microRNA, mouse)
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - 0 (NF-kappa B)
RN  - 0 (Toll-Like Receptor 2)
SB  - IM
MH  - 3' Untranslated Regions/genetics
MH  - Animals
MH  - Autophagy/*genetics
MH  - Base Sequence
MH  - Gene Expression Regulation
MH  - Intracellular Space/microbiology
MH  - Macrophages/metabolism/microbiology
MH  - Mice
MH  - MicroRNAs/genetics/*metabolism
MH  - *Microbial Viability
MH  - Mycobacterium tuberculosis/*physiology
MH  - Myeloid Differentiation Factor 88/*metabolism
MH  - NF-kappa B/*metabolism
MH  - Protein Binding/genetics
MH  - RAW 264.7 Cells
MH  - Signal Transduction
MH  - Toll-Like Receptor 2/genetics/*metabolism
MH  - Tuberculosis/*genetics/immunology/microbiology/pathology
OTO - NOTNLM
OT  - Autophagy
OT  - Mycobacterium tuberculosis (M.tb.)
OT  - TLR2/MyD88/NF-kappaB pathway
OT  - miR-23a-5p
EDAT- 2017/03/23 06:00
MHDA- 2017/07/14 06:00
CRDT- 2017/03/23 06:00
PHST- 2016/12/10 00:00 [received]
PHST- 2017/02/20 00:00 [revised]
PHST- 2017/03/14 00:00 [accepted]
PHST- 2017/03/23 06:00 [pubmed]
PHST- 2017/07/14 06:00 [medline]
PHST- 2017/03/23 06:00 [entrez]
AID - S0014-4827(17)30151-9 [pii]
AID - 10.1016/j.yexcr.2017.03.039 [doi]
PST - ppublish
SO  - Exp Cell Res. 2017 May 15;354(2):71-77. doi: 10.1016/j.yexcr.2017.03.039. Epub 
      2017 Mar 19.